INTRODUCTION

Historically, epilepsy has been neglected, feared, and misunderstood. A veil of

secrecy surrounding the disease has resulted in myths, superstitions, and a general lack of
knowledge. This has impeded scientific progress toward finding answers to one of the oldestknown and most prevalent neurological diseases, leaving treatment and research efforts in the
dark ages.
There is an increasingly large incidence of new onset epilepsy in the aging population as a result
of strokes, brain tumors, and Alzheimer's Disease. In addition, for many soldiers suffering
traumatic brain injury on the battlefield, epilepsy will be a long-term consequence.

DEFINITION
An epileptic seizure is electrophysiologically characterized by abnormal transient and
excessive electrical discharge of cerebral neurons and clinically characherised by paroxysmal
episodes of loss or excess of motor, sensory,autonomic or psychic functions with or without
alteration in consciousness.
According to ILAE task epilepsy be considered to be a disease of the brain characterized
by any of the following conditions: at least two unprovoked (or reflex) seizures occurring >24
hours apart; one unprovoked (or reflex) seizure and a probability of further seizures similar to the
general recurrence risk (at least 60 percent) after two unprovoked seizures, occurring over the
next 10 years; or diagnosis of an epilepsy syndrome. For individuals who either had an agedependent epilepsy syndrome but are now past the applicable age or who have remained seizurefree for the last 10 years and off anti-seizure medicines for at least the last five years, epilepsy is
considered resolved. "Resolved" may not be the same as the conventional view of "remission" or
"cure."
In other words seizure is a symptom and epilepsy is a syndrome. Though epilepsy begins first
with a seizure, not all first seizures lead to epilepsy. Seizures may often occur in acute systemic
conditions such as metabolic disturbances (hypoglycemia), drug toxicity (chloroquine) and drug
withdrawal (diazepam) but usually they do not constitute epilepsy.

Incidence and prevalence

* A house to house study done on 25000 persons in Central Travancore gave the prevalence
rate as 5/1,000 of persons
*The International League Against Epilepsy gives the incidence as 50-100/100,000
population

*65 MILLION: Number of people around the world who have epilepsy.
*ONE-THIRD: Number of people with epilepsy who live with uncontrollable seizures
because no available treatment works for them.
*6 OUT OF 10: Number of people with epilepsy where the cause is unknown.
(epileptic foundation)

ETIOLOGY OF EPILEPSY
In about 70% of cases of epilepsy, no cause can be determined even after extensive
investigations (primary or idiopathic epilepsy). In the remaining group the etiology varies and is
multifactorial depending upon the age of onset and the type of epilepsy. The causes include a
large variety of genetically determined, congenital and acquired conditions.
Certain clinical observations emphasize how a variety of factors determine why certain
conditions may cause seizures or epilepsy in a given patient
1. The normal brain is capable of having a seizure under the appropriate circumstances,
and there are differences between individuals in the susceptibility or threshold for
seizures. For example, seizures may be induced by high fevers in children who are
otherwise normal and who never develop other neurologic problems, including epilepsy.
However, febrile seizures occur only in a relatively small proportion of children. This
implies there are various underlying endogenous factors that influence the threshold for
having a seizure. Some of these factors are clearly genetic, as it has been shown that a
family history of epilepsy will influence the likelihood of seizures occurring in otherwise
normal individuals. Normal development also plays an important role, since the brain
appears to have different seizure thresholds at different maturational stages.
2. There are a variety of conditions that have an extremely high likelihood of resulting in a
chronic seizure disorder. One of the best examples of this is severe, penetrating head
trauma, which is associated with up to a 50% risk of subsequent epilepsy. The high
propensity for severe traumatic brain injury to lead to epilepsy suggests that the injury
results in a long-lasting pathologic change in the CNS that transforms a presumably
normal neural network into one that is abnormally hyperexcitable. This process is known
as epileptogenesis, and the specific changes that result in a lowered seizure threshold can
be considered epileptogenic factors. Other processes associated with epileptogenesis
include stroke, infections, and abnormalities of CNS development. Likewise, the genetic
abnormalities associated with epilepsy likely involve processes that trigger the
appearance of specific sets of epileptogenic factors.

3. Seizures are episodic. Patients with epilepsy have seizures intermittently and, depending
on the underlying cause, many patients are completely normal for months or even years
between seizures. This implies there are important provocative or precipitating factors
that induce seizures in patients with epilepsy. Similarly, precipitating factors are
responsible for causing the single seizure in someone without epilepsy. Precipitants
include those due to intrinsic physiologic processes, such as psychological or physical
stress, sleep deprivation, or hormonal changes associated with the menstrual cycle. They
also include exogenous factors such as exposure to toxic substances and certain
medications.

Table 363-4 Causes of Seizures

Neonates (<1 month)

Perinatal hypoxia and ischemia

Intracranial hemorrhage and trauma
Acute CNS infection
Metabolic
disturbances
(hypoglycemia,
hypomagnesemia, pyridoxine deficiency)

hypocalcemia,

Drug withdrawal
Developmental disorders
Genetic disorders
Infants and children (>1 mo and Febrile seizures
<12 years)
Genetic disorders
syndromes)

(metabolic,

CNS infection
Developmental disorders
Trauma
Idiopathic
Adolescents (1218 years)

Trauma
Genetic disorders
Infection
Brain tumor
Illicit drug use

degenerative,

primary

epilepsy

Idiopathic
Young adults (1835 years)

Trauma
Alcohol withdrawal
Illicit drug use
Brain tumor
Idiopathic

Older adults (>35 years)

Cerebrovascular disease
Brain tumor
Alcohol withdrawal
Metabolic disorders (uremia, hepatic failure, electrolyte abnormalities,
hypoglycemia)
Alzheimer's disease and other degenerative CNS diseases
Idiopathic

PATHOGENESIS
A seizure occurs when a portion of the brain becomes overly excited or when nerves in the
brain begin to fire together in an abnormal fashion. Seizure activity can arise in areas of the brain
that are malformed from birth defects or genetic disorders or disrupted from infection, injuries,
tumors, strokes, or inadequate oxygenation
. The pathophysiology of seizures results from an abrupt imbalance between the forces that
excite and inhibit the nerve cells such that the excitatory forces take precedence. This electrical
signal then spreads to the surrounding normal brain cells, which begin to fire in concert with the
abnormal cells. With prolonged or recurrent seizures over a short period, the risk of future
seizures increases as nerve cell death, scar tissue formation, and sprouting of new axons
occur.Nerve cells between discharges normally have a negative charge internally due to the
active pumping of positively charged sodium ions out of the cell. Discharge or firing of the nerve
cell involves a sudden fluctuation of the negative charge to a positive charge as ions channels
into the cell open and positive ions, such as sodium, potassium, and calcium, flow into the cell.
Both excitatory and inhibitory control mechanisms act to allow appropriate firing and prevent
inappropriate excitation of the cell. The pathophysiology of seizures can occur due to increased
excitation of the nerve cell, decreased inhibition of the nerve cell, or a combination of both
influences. Normally after a nerve cell fires, inhibitory influences prevent a second firing of the

neuron until the internal charge of the neuron returns to its resting state. Gamma-amino-butyric
acid (GABA) is the principal inhibiting chemical in the brain. GABA opens channels for
negatively charged chloride ions to flood into the excited neuron, which decreases the internal
charge and prevents a second firing of the nerve cell. Most anti-seizure drugs reduce the
pathophysiology of seizures by increasing the frequency of the chloride channel openings or
increasing the duration during which the channels are open. When there is a disruption in the
cells that issue GABA or the receptor sites for GABA, there is a failure of the chloride channels
to open and temper the excitability of the nerve cell.Equally significant to the pathophysiology of
seizures are mechanisms that lead to increased excitation of neurons. Glutamate is the main
excitatory chemical mediator in the brain, which binds to receptors that open channels for
sodium, potassium, and calcium into the cell.
Some inherited forms of seizures involve a predilection for excessively frequent or
sustained activation of glutamate receptors, increasing the excitability of the brain and the
prospect for seizure activity. Furthermore, contiguous spread of the electrical activity along
layered parts of the brain may occur from cell to cell, a non-chemical form of propagation that is
not subject to regulation by inhibitory mechanisms.
Treatments for the pathophysiology of seizures target not only the molecular
abnormalities involving the ion channels in the nerve cells but also the non-chemical spreading
of excitation in the brain. Benzodiazepines, such as Valium, and barbiturates, such as
Phenobarbital, act to open inhibitory chloride channels. Phenytoin or Dilantin prevents repetitive
firing of neurons by shutting down sodium channels into the nerve cells. In situations with poorly
managed recurrent seizures, halothane may prevent the non-chemical transmission of nerve
impulses. Additionally, insulin and steroids change the function of glutamate receptors,
suppressing the excitability of the brain.

TYPES
1. Classification of epileptic seizures: This is largely based on the seizure type and to a lesser
extent on EEG findings. In this classification, seizures are divided into two main categories
depending upon the location of the initial epileptic discharge in the brain, i.e. localized to a small
area (partial seizures) or larger areas in both hemispheres (generalised seizures).
2. Classifications of epilepsies and epileptic syndromes:This is based on clinical manifestations,
age of onset, genetic predisposition, associated neurological and other abnormalities and overall
prognosis.

Classification of Epileptic Seizures

Generalised Seizures

A. Absence seizures
B. Myoclonic seizures
C. Clonic seizures
D. Tonic seizures
E. Tonic-clonic seizures
F. Atonic seizures
Partial Seizures
A. Simple partial seizures
1. with motor manifestations
2. with somatosensory or special sensory manifestations
3. with autonomic manifestations
4. with psychic manifestations.
B. Complex partial seizures
1. with simple partial features at onset followed by impairment of consciousness
2. with impairment of consciousness at onset.
C. Partial seizures evolving to secondarily generalized seizures
1simple partial seizure generalised seizure
2. complex partial seizure generalised seizure
3. simple partial seizure complex partial seizure generalised seizure.

CLASSIFICATION OF EPILEPSIES AND

EPILEPTIC SYNDROMES
1. Localization related (focal, local, partial)
epilepsies syndromes
Temporal lobe epilepsies
Frontal lobe epilepsies
Parietal lobe epilepsies
Occipital lobe epilepsies
2.Generalized epileptic syndromes
Lennox-Gastaut syndrome
Epilepsy with myoclonic/astatic seizures
Epilepsy with myoclonic absences.

PARTIAL SEIZURES
Partial seizures or focal seizures are due to a small epileptic focus in the brain. They are
divided into two main categories.a. simple partial seizure in which the seizure starts as a focal

discharge and remains focal throughout without alteration of consciousness and b. complex
partial seizure when a seizure starts as a focal discharge, but consciousness is also altered or lost.

Simple Partial Seizures

These seizures may have motor, sensory, autonomic or psychic manifestations.Simple focal or
partial motor seizures are due to a discharging epileptic focus in the opposite frontal lobe (motor
cortex). These consist of clonic movements of the hand, foot or angle of mouth or turning of the
head or eyes. These movements may constitute the entire motor component of the seizure or may
be followed by generalised clonic movements and loss of consciousness. The term jacksonian
motor seizures (Jacksonian epilepsy)is applied to the type where clonic contractions start in the
fingers of one hand, one side of the face or the foot and slowly spread (march) to the other
muscles on the same side of the body. This may or may not be followed consciousness. The
presence of the characteristic march distinguishes Jacksonian seizures from partial motor
seizures. However, both have the same localizing significance.

Complex Partial Seizures

(Psychomotor Epilepsy)
These are defined as focal or partial seizures in which consciousness is
impaired or lost. They are frequently due to epileptic discharges in the temporal or frontal lobes.
Less commonly they may arise from discharges in other parts of the brain. This forms the single
most common type of seizure in adults. The seizure usually consists of complex hallucination of
perceptual illusions, indicating its origin from the temporal lobe. The hallucinations are usually
auditory and visual but sometimes they may be olfactory or gustatory. The subjects may show
increased familiarity (dj vu) or unfamiliarity ( jamais vu) with the surroundings. In some cases
these subjective experiences may constitute the entire seizure. Often this is followed by a period
of unresponsiveness, during which the patient exhibits certain automatic behaviour like smacking
of the lips or chewing movements (automatism). The patient may walk about or repeat a habitual
act. However, when asked a question the unresponsiveness becomes evident. Sometimes
unprovoked aggression or laughter may be the striking feature. The automatism usually lasts for
a few minutes, but may sometimes be prolonged. The patient is totally amnesic for the whole
period of automatism. The EEG recorded during sleep or hyperventilation may demonstrate the
temporal lobe focus. Rarely, other areas of brain like the orbital surface of the frontal lobe or
limbic system may be seat of epileptic discharge.

Partial Seizures Evolving to Secondarily

Generalised Seizures
In many cases the generalised seizures are not generalized from their onset. They start as
partial seizures, either bysimple or complex and then soon spread to become generalised, usually
as tonic clonic convulsions. These are called partial seizures becoming secondarily generalised.In
such cases the initial manifestations of partial seizures are called aura or warning symptoms.

PRIMARY GENERALISED EPILEPSIES

Primary Generalised SeizuresThese are seizures in which there is no evidence of an epileptic
focus, either clinically or on EEG, as opposed to secondary generalised seizures. The epileptic

discharge involves both cerebral hemispheres simultaneously from the onset of the seizures.
Hence, consciousness is almost invariably impaired or lost at the onset of the attack.Generalised
seizures are divided into several clinical types and some patients may suffer from more than one
seizure type. Atypical seizure patterns may also occur, especially if the patient is on treatment.
Tonic Clonic Seizures
These are also called grand mal epilepsy.The seizure attack occurs in different stages
sequentially. The stages may be subdivided into the prodromal phase, tonic phase, clonic phase
and the postictal phase. The prodromal phase may start several hours before the ictus (fit). It
consists of several subjective phenomena like depressed or apathetic mood, irritability, vague
abdominal cramps or other funny sensations, which are easily recognised by the patient. In many
instances there is no aura and the patient gets the attack without any forewarning. Presence of
aura suggests the nature of the seizure as of focal onset (i.e.) partial seizure.The tonic phase
consists of rolling up of the eyes associated with stiffening of the limbs followed by clenching of
the jaws, often resulting in injury to the tongue. The attack may be heralded by an epileptic cry
as the entire musculature goes into spasm forcing air through the closed vocal cords. The patient
becomes cyanosed due to spasm of respiratory muscles. This phase lasts for about 10 to 30
seconds. The tonic phase is followed by clonic phase characterized by alternate flexion-extension
movements of all the four limbs (convulsions), strenuous breathing, sweating, frothing of the
mouth and excess salivation. Urine and feces may be voided. The clonic phase usually lasts for
1-2 minutes. This is followed by a deep comatose state, which lasts for about 5 minutes. The
pupils slowly begin to react and the patient then resumes speech, but still remains confused. If
left undisturbed, he goes into sleep for several hours and often wakes up with severe headache
and at times, vomiting. This is the post-ictal phase and the patient does not remember anything
that had happened. Electroencephalogram (EEG) taken during the attack or sometimes even
during the intervals shows generalized seizure discharges. The EEG is often normal in the
interictal period.

Absence Seizures (Petit Mal)

These are seen mostly in children. These are distinguished by brevity and absence of motor
phenomena. The child does not fall. The attacks come on without any warning and consciousness
is impaired only for a brief period often < 10 seconds. The child abruptly stops all ongoing motor
activity and speech. There is a vacant stare. Ex stimuli fail to evoke any response from the
patient at thatperiod. These attacks usually last for 2-10 sec after whichthe patient resumes the
pre-seizure activity. At times there may be clonic movements of the eyelids or occasionally
automatisms like smacking of lips or chewing movements. The attacks can be precipitated by
hyperventilation. The attacks occur several times during the day, but theynbecome less frequent
or may even disappear in adolescence. Sometimes these may be replaced by tonicclonic seizures.
The EEG abnormality in petit mal epilepsy is diagnostic. It shows classic three per second
spike and wave generalised discharges
.

Atonic Seizures
These are less common generalised seizures characterized by sudden loss of postural tone and
consciousness without any other motor phenomena. This may lead to sudden drop of the
individual to the floor without any warning. Atonic seizures have to be distinguished from
cataplexy in which the drop attacks are not accompanied by loss of consciousness and syncope.

EPILEPTIC SYNDROMES
Juvenile Myoclonic Epilepsy
Juvenile myoclonic epilepsy (JME) is the most common of the generalized epilepsy
syndromes to emerge in early adolescence and is usually characterized by bilateral myoclonic
jerks that may be single or repetitive . The hallmark characteristics of juvenile myoclonic
epilepsy are the presence of myoclonic jerks that occur on awakening from sleep either in the
morning. They are typically described as shock-like, irregular and arrhythmic movements of both
arms. Sometimes these movements are restricted only to the fingers making the patient or
individual look clumsy or prone to dropping things.
Juvenile myoclonic epilepsy is a genetically determined syndrome. About 50-60% of
families with juvenile myoclonic seizures report seizures in either a direct relative or a cousin.
The inheritance is of a complex type, although there are certain subtypes that have distinct
genetic patterns associated with it. One of the most interesting aspects of juvenile myoclonic
epilepsy is the fact that there are two very common seizure-precipitating factors - sleep
deprivation and stress. Sleep deprivation and fatigue, primarily after excessive alcohol intake, are
the most powerful precipitants of myoclonic jerks and generalized tonic-clonic seizures in JME

Lennox-Gastaut Syndrome (LGS)

The Lennox-Gastaut syndrome (LGS) is a type of epilepsy with multiple different types of
seizures, particularly tonic (stiffening) and atonic (drop) seizures. Intellectual development is
usually, but not always, impaired. The EEG shows a classic pattern of background slowing and
spike-wave bursts at frequencies less than 2.5 per second. The cause of the disorder is unknown
in 1 out of 4 children.
Lennox-Gastaut syndrome is associated with CNS disease or dysfunction from a variety of
causes ,including developmental abnormalities ,perinatal hypoxia ,trauma ,infection and other
acquired lesions. Treatment is difficult, because the seizures often don't respond to seizure
medications or AEDs. The intellectual changes do not respond to any currently available
medicine or treatment either.

Rasmussen's Syndrome
Rasmussen's syndrome is associated with slowly worsening neurological problems and seizures
in children. Seizures are often the first problem to appear. Simple partial motor seizures are the
most common type, but in 1 out of 5 children, the first seizure is an episode of partial or tonicclonic status epilepticus.
Mild weakness of an arm or leg is the most common early symptom besides seizures.The
weakness and other neurological problems often begin 1 to 3 years after the seizures
start.Progressive weakness on one side (hemiparesis) and thinking/memory impairment are
common.Language problems (aphasia) often occur if the disorder affects the side of the brain
that controls most language functions, which is usually the left side. Rasmussen's syndrome
usually begins between 14 months and 14 years of age. Recent studies suggest that the cause of
Rasmussen's syndrome is an autoimmune disorder (antibodies are produced against the body's
own tissues) directed against receptors on the brain cells. Treatment of this disease with seizure
medicines is disappointing. Anti-inflammatory steroids may be effective, but additional studies
are needed. Immunologic therapies (gamma globulin, plasmapheresis, rituximab) may be helpful
in some cases.
TEMPORAL LOBE EPILEPSY
Temporal lobe epilepsy is the most common form of partial or localization related epilepsy
The features of seizures beginning in the temporal lobe can be extremely varied, but certain
patterns are common. Hallucinations of voices, music, people, smells, or tastes may occur. These
features are called auras or warnings. They may last for just a few seconds, or may continue
as long as a minute or two. Medial temporal lobe epilepsy often begins within a structure of the
brain called the hippocampus or its surrounding structures. It accounts for almost 80% of all
temporal lobe seizures. While medial temporal lobe epilepsy is a very common form of epilepsy,
it is also frequently resistant to medications and associated with a particular finding on an MRI.
This finding is called hippocampal sclerosis (sclerosis means hardening) and it makes this a
challenge to treat both medically and oftentimes surgical therapy is the best option for these
individuals

Dravet Syndrome
Dravet Syndrome is a rare genetic epileptic encephalopathy (dysfunction of the brain). It
begins in the first year of life in an otherwise healthy infant. Prior to 1989, this syndrome was
known as epilepsy with polymorphic seizures, polymorphic epilepsy in infancy (PMEI) or severe

myoclonic epilepsy in infancy (SMEI). The disease begins in infancy but is lifelong. Myoclonic
seizures
Tonic clonic seizures
Absence seizures
Atypical absence seizures
Atonic seizures
Partial seizures
Non-convulsive status epilepticus Diagnosing the child early is critical to proper treatment
and achieving the best outcome.A multidisciplinary team is needed to address the many ways
that Dravet Syndrome can affect a child and their family.Seizure treatment is aimed at finding the
best combination of medicines to treat seizures chronically and prevent and treat potential
seizure emergencies.Getting the best seizure control possible is the goal. This could also help
improve the childs developmental abilities and decrease mortality risk

DIAGNOSIS
When a patient presents shortly after a seizure, the first priorities are attention to vital
signs, respiratory and cardiovascular support, and treatment of seizures if they resume (see
"Seizures and Epilepsy: Treatment"). Life-threatening conditions such as CNS infection,
metabolic derangement, or drug toxicity must be recognized and managed appropriately.
When the patient is not acutely ill, the evaluation will initially focus on whether there is a history
of earlier seizures. If this is the first seizure, then the emphasis will be to (1) establish whether
the reported episode was a seizure rather than another paroxysmal event, (2) determine the cause
of the seizure by identifying risk factors and precipitating events, and (3) decide whether
anticonvulsant therapy is required in addition to treatment for any underlying illness.
In the patient with prior seizures or a known history of epilepsy, the evaluation is directed toward
(1) identification of the underlying cause and precipitating factors, and (2) determination of the
adequacy of the patient's current therapy.

History and Examination

CNS disease. Precipitating factors such as sleep deprivation, systemic diseases, electrolyte or
metabolic derangements, acute infection, drugs that lower the seizure threshold (Table 363-5), or
alcohol or illicit drug use should also be identified.
The general physical examination includes a search for signs of infection or systemic illness.
Careful examination of the skin may reveal signs of neurocutaneous disorders, such as tuberous
sclerosis or neurofibromatosis, or chronic liver or renal disease. A finding of organomegaly may
indicate a metabolic storage disease, and limb asymmetry may provide a clue to brain injury
early in development. Signs of head trauma and use of alcohol or illicit drugs should be sought.
Auscultation of the heart and carotid arteries may identify an abnormality that predisposes to
cerebrovascular disease.
All patients require a complete neurologic examination, with particular emphasis on eliciting
signs of cerebral hemispheric disease (Chap. 361). Careful assessment of mental status
(including memory, language function, and abstract thinking) may suggest lesions in the anterior
frontal, parietal, or temporal lobes. Testing of visual fields will help screen for lesions in the
optic pathways and occipital lobes. Screening tests of motor function such as pronator drift, deep
tendon reflexes, gait, and coordination may suggest lesions in motor (frontal) cortex, and cortical
sensory testing (e.g., double simultaneous stimulation) may detect lesions in the parietal cortex.

Laboratory Studies
Routine blood studies are indicated to identify the more common metabolic causes of seizures,
such as abnormalities in electrolytes, glucose, calcium, or magnesium, and hepatic or renal
disease. A screen for toxins in blood and urine should also be obtained from all patients in The
first goal is to determine whether the event was truly a seizure. An in-depth history is essential,
for in many cases the diagnosis of a seizure is based solely on clinical groundsthe examination
and laboratory studies are often normal
The history should also focus on risk factors and predisposing events. Clues for a predisposition
to seizures include a history of febrile seizures, earlier auras or brief seizures not recognized as
such, and a family history of seizures. Epileptogenic factors such as prior head trauma, stroke,
tumor, or infection of the nervous system should be identified. In children, a careful assessment
of developmental milestones may provide evidence for underlyingappropriate risk groups,
especially when no clear precipitating factor has been identified. A lumbar puncture is indicated
if there is any suspicion of meningitis or encephalitis, and it is mandatory in all patients infected
with HIV, even in the absence of symptoms or signs suggesting infection.

Electrophysiologic Studies
All patients who have a possible seizure disorder should be evaluated with an EEG as soon as
possible.
In the evaluation of a patient with suspected epilepsy, the presence of electrographic seizure
activity during the clinically evident eventi.e., abnormal, repetitive, rhythmic activity having
an abrupt onset and terminationclearly establishes the diagnosis. The absence of
electrographic seizure activity does not exclude a seizure disorder, however, because simple or
complex seizures may originate from a region of the cortex that is not within range of the scalp
electrodes. The EEG is always abnormal during generalized tonic-clonic seizures. Since seizures
are typically infrequent and unpredictable, it is often not possible to obtain the EEG during a
clinical event. Continuous monitoring for prolonged periods in video-EEG telemetry units for
hospitalized patients or the use of portable equipment to record the EEG continuously on
cassettes for 24 h in ambulatory patients has made it easier to capture the electrophysiologic
accompaniments of clinical events. In particular, video-EEG telemetry is now a routine approach
for the accurate diagnosis of epilepsy in patients with poorly characterized events or seizures that
are difficult to control

Brain Imaging
Almost all patients with new-onset seizures should have a brain imaging study to determine
whether there is an underlying structural abnormality that is responsible. The only potential
exception to this rule is children who have an unambiguous history and examination suggestive
of a benign, generalized seizure disorder such as absence epilepsy. MRI has been shown to be
superior to CT for the detection of cerebral lesions associated with epilepsy. In some cases MRI
will identify lesions such as tumors, vascular malformations, or other pathologies that need
immediate therapy. The use of newer MRI methods, such as fluid-attenuated inversion recovery
(FLAIR), has increased the sensitivity for detection of abnormalities of cortical architecture,
including hippocampal atrophy associated with mesial temporal sclerosis, as well as
abnormalities of cortical neuronal migration. In such cases the findings may not lead to
immediate therapy, but they do provide an explanation for the patient's seizures and point to the
need for chronic anticonvulsant therapy or possible surgical resection.
In the patient with a suspected CNS infection or mass lesion, CT scanning should be performed
emergently when MRI is not immediately available. Otherwise, it is usually appropriate to obtain
an MRI study within a few days of the initial evaluation. Functional imaging procedures such as
positron emission tomography (PET) and single photon emission computed tomography
(SPECT) are also used to evaluate certain patients with medically refractory seizures

Treatment
MANAGEMENT OF EPILEPSY
This consists of (i) treatment of the acute convulsions,
and (ii) prophylactic management of convulsive and nonconvulsive
seizures.
The latter consists of :
1. Removal of precipitating or causative factors.
2. Antiepileptic medication.
3. Social rehabilitation.
Mgmnt Acute Convulsion
Convulsion is a medical emergency especially if prolonged, which should be arrested
without delay. The patient is put on a soft bed to avoid injuries, tight clothing is loosened and the
airway is protected so as to avoid asphyxiation and aspiration. Dentures and foreign bodies in the
mouth should be removed and a suitable mouth gag is applied in the position of the molar teeth,
to keep the mouth open and prevent injury to the tongue. The patient should be kept with head
low, so as to avoid aspiration of vomitus into the respiratory tract. Most convulsions are selflimited and need no immediate treatment. However, prolonged or recurring convulsion should be
controlled by slow intravenous injection of 5-10 mg or more of diazepam. An alternate
anticonvulsant drug is lorazepam 4 mg IV given slowly over 5-10 minutes. Other drug that must
be given parenterally is phenytoin sodium 100-200 mg IV. This helps to prevent recurrence as
well. The physician may encounter the patient with convulsions in the most embarrassing
situations,and therefore, the first injection of anticonvulsant medication may have to be given IV
in order to terminate the convulsion forthwith, fully realising the risk involved. Adverse drug
effects include anaphylaxis, respiratory depression, hypotension and allergic manifestations.
Once the convulsions are controlled, further management has to be carefully planned. Failure to
arrest the convulsions leads to asphyxia, severe exhaustion, hyperpyrexia, electrolyte imbalance,
further cerebral damage and death. All cases of convulsions should be investigated for the
presence of primary or secondary neurological conditions giving rise to symptomatic seizure.
Conditions like meningitis, encephalitis, neurosyphilis, neurocysticercosis, fluid and electrolyte
imbalance, hypocalcemia, abnormal glucose levels and intracranial space occupyinglesions have
to be excluded.

TREATMENT OF UNDERLYING CONDITIONS

If the sole cause of a seizure is a metabolic disturbance such as an abnormality of serum

electrolytes or glucose, then treatment is aimed at reversing the metabolic problem and
preventing its recurrence. Therapy with antiepileptic drugs is usually unnecessary unless the
metabolic disorder cannot be corrected promptly and the patient is at risk of having further
seizures. If the apparent cause of a seizure was a medication (e.g., theophylline) or illicit drug
use (e.g., cocaine), then appropriate therapy is avoidance of the drug; there is usually no need for
antiepileptic medications unless subsequent seizures occur in the absence of these precipitants.

Avoidance of Precipitating Factors

Unfortunately, little is known about the specific factors that determine precisely when a
seizure will occur in a patient with epilepsy. Some patients can identify particular situations that
appear to lower their seizure threshold; these situations should be avoided. For example, a
patient who has seizures in the setting of sleep deprivation should obviously be advised to
maintain a normal sleep schedule. Many patients note an association between alcohol intake and
seizures, and they should be encouraged to modify their drinking habits accordingly. There are
also relatively rare cases of patients with seizures that are induced by highly specific stimuli such
as a video game monitor, music, or an individual's voice ("reflex epilepsy"). If there is an
association between stress and seizures, stress reduction techniques such as physical exercise,
meditation, or counseling may be helpful.

ANTIEPILEPTIC DRUG THERAPY

.

Though AEDs are not curative in epilepsy , they help to control seizures and give
symptomatic relief. In many instances prolonged administration results in abolition of the
epileptic tendency. The response varies in the different types of seizures and hence it is necessary
to administer the appropriate AED in optimum dosage. The present consensus is to start with a
single drug and add others later on, only when absolutely necessary. The first line AEDs are the
time tested drugs such as phenytoin, phenobarbitone, primidone, carbamazepine,
ethosuximide,sodium valproate, and clonazepam. At present oxcarbazepine, topiramate and
lamotrigine are also increasingly used as first line drugs .If the response to a single drug is not
adequate, another drug should be added. In some the combination produces better effect. A
stable drug regimen should not, however, be frequently changed. Sudden withdrawal of
AED should be avoided since this is the most common cause for precipitation of status
epilepticus.

Indications for starting antiepileptic therapy: When more than one unprovoked seizure has
occurred in the preceding one to two years or when the risk of recurrent convulsionis high as in
head injury or intracranial infections. AED should be started. Since the medication has to be
prolonged and the drugs are potentially toxic and expensive, patients with single attack without
demonstrable focal abnormalities either clinically or on investigations such as EEG, CT or MRI,
the patient should be observed and therapy started only if seizures recur.
Guidelines for AED Therapy
1. Start with a single drug and adjust its dosage to achieve maximal clinical benefit without side
effects.
2. If seizures occur even after achieving tolerable dose of the single drug a second drug should be
introduced and the first one slowly withdrawn.
3. Different combinations of two drugs may be tried, each trial lasting for a maximum of six
months, till the ideal combination is arrived at. There is no role for combining more than two
drugs.
4. Therapy should continue till at least a 3-year seizure free period is completed after which the
drugs can be gradually withdrawn. Nearly 50% of the patients may not require any further
treatment. The rest may elapse and this usually occurs within five years. Children who develop
primary epilepsy in early life and who show prompt response to AED have greater chance for
permanent remission.
5. Twenty-five percent of cases may develop chronic epilepsy and require life-long medication.
Risk of chronicity is high in patients with neurological and psychological abnormalities and
social handicaps. Partial seizures are more refractory to medical treatment in upto 20% of cases.
These may require surgery. When confronted with intractable seizures, newer drugs should be
considered. Before doing so it is wise to verify the following:
1. Is the diagnosis correct.
2. Is the epilepsy secondary to other disease processes.
3. Are the appropriate drugs taken regularly and in full doses.
4. Are there any adverse psychosocial factors.

Details

of

the

commonly

used

anticonvulsant-drugs

Newer Antiepileptic Drugs

Several newer antiepileptic drugs are on the anvil. Many of these are now freely available in
India. At present, these newer drugs are recommended as add-on drugs along with conventional
drugs, to treat intractable cases, although some of them are found effective as initial
monotherapy.
Vigabatrin: Gamma vinyl GABA (GVG): This drug irreversibly inhibits GABA
aminotransferase.
Dose: 50-100 mg/kg/day.
Indications: Complex partial seizures with secondary generalisation, infantile spasms. Adverse
effects are mild. These include defects in the visual fields, sedation and behavioural disturbances.
Zonisamide: This is a benzisoxazole derivative.
Dose: 6-10 mg/kg/day. The initial dose is 100 mg/day.
Indications: Partial seizures with secondary generalisation, primary generalised tonic-clonic,
atonic and myoclonic seizures. Adverse effects include feverishness, ataxia, leucopenia and
urinary calculi.
Oxcarbazepine: This is chemically related to carbamazepine.
Its action is similar to carbamazepine but this drug is better tolerated. Ataxia is the main adverse
effect.
Dose: 1200-2400 mg/day.
Gabapentin(Neurontin): This is a GABA-related amino acid with broad spectrum anti-epileptic
activity.
Dose: The initial daily dose is 300 mg increased to 600 to 1300 mg over a few days. Even doses
as high as 3600 mg/day are safe. This drug is well tolerated and the full dose can be attained
within 3-4 days. It can be safely possible.
When to Discontinue Therapy

Overall, about 70% of children and 60% of adults who have their seizures completely
controlled with antiepileptic drugs can eventually discontinue therapy. The following patient
profile yields the greatest chance of remaining seizure-free after drug withdrawal: (1)complete
medical control of seizures for 15 years; (2) single seizure type, either partial or generalized;
(3) normal neurologic examination, including intelligence; and (4) normal EEG. The appropriate
seizure-free interval is unknown and undoubtedly varies for different forms of epilepsy.
However, it seems reasonable to attempt withdrawal of therapy after 2 years in a patient who
meets all of the above criteria, is motivated to discontinue the medication, and clearly
understands the potential risks and benefits. In most cases it is preferable to reduce the dose of
the drug gradually over 23 months. Most recurrences occur in the first 3 months after
discontinuing therapy, and patients should be advised to avoid potentially dangerous situations
such as driving or swimming during this period.

Surgical Management of Epilepsy

Lobe resection:Temporal lobe epilepsy, in which the seizure focus is located within

the temporal lobe, is the most common type of epilepsy in teens and adults. In a temporal
lobe resection, brain tissue in the temporal lobe is resected, or cut away, to remove the
seizure focus. The anterior (front) and mesial (deep middle) portions of the temporal lobe are
the areas most often involved. Extratemporal resection involves removing brain tissue from
areas outside of the temporal lobe.

Lesionectomy: This is surgery to remove isolated brain lesions -- areas of injury or

defect such as a tumor or malformed blood vessel -- that are responsible for seizure activity.
Seizures usually stop once the lesion is removed.

Corpus callosotomy: The corpus callosum is a band of nerve fibers connecting the
two halves (hemispheres) of the brain. A corpus callosotomy is an operation in which all or
part of this structure is cut, disabling communication between the hemispheres and

preventing the spread of seizures from one side of the brain to the other. This procedure,
sometimes called split-brain surgery, is for patients with extreme forms of uncontrollable
epilepsy who have intense seizures that can lead to violent falls and potentially serious
injury.

Functional hemispherectomy: This is a variation of a hemispherectomy, a radical

procedure in which one entire hemisphere, or one half of the brain, is removed. With a
functional hemispherectomy, one hemisphere is disconnected from the rest of the brain, but
only a limited area of brain tissue is removed. This surgery generally is limited to children
younger than 13 years old who have one hemisphere that is not functioning normally.

Multiple subpial transection (MST): This procedure is used to help control seizures
that begin in areas of the brain that cannot be safely removed. The surgeon makes a series of
shallow cuts (transections) in the brain tissue. These cuts interrupt the movement of seizure
impulses but do not disturb normal brain activity, leaving the person's abilities intact.

Vagus nerve stimulation (VNS): This is a device that electronically stimulates the
vagus nerve (which controls activity between the brain and major internal organs) is
implanted under the skin. This reduces seizure activity in some patients with partial seizures.

Responsive neurostimulation device (RNS): This device consists of a small

neurostimulator implanted within the skull under the scalp. The neurostimulator is connected
to one or two wires (called electrodes) that are placed where the seizures are suspected to
originate within the brain or on the surface of the brain. The device detects abnormal
electrical activity in the area and delivers electrical stimulation to normalize brain activity
before seizure symptoms begin.

Status Epilepticus
When recurrent seizures occur at a frequency which does not allow consciousness to be
regained in the interval between seizures, it is called status epilepticus. Severe and permanent
brain damage may result from status epilepticus persisting for more than an hour. Since
prolonged or frequent seizures also lead to permanent damage to the brain (hippocampus,
Purkinje cells of cerebellum and extrapyramidal system) it is the current consensus to consider
any seizure (both clinical or electrical) lasting for more than 30 minutes, or more than one
seizure within 30 minutes even if consciousness is not lost, as status epilepticus, for purposes of
management.
Status epilepticus may be convulsive or nonconvulsive.Convulsive status which may be partial
or generalised may be tonic, clonic, or myoclonic types and secondary generalised forms.

Nonconvulsive status (absence status) or complex partial status may vary from simple slowingof
ideas to marked stupor from which the patient can be woken up only be painful stimuli.
Nonconvulsive statuscan be diagnosed only by EEG recordings. Such patients are also prone to
develop damage to the brain
Management

Time is a critical factor in the management of status epilepticus. There are many therapeutic
regimes but none of them is totally satisfactorily. Benzodiazepines such as diazepam, lorazepam,
midazolam and clonazepam are all potent fast-acting antiepileptic drugs, preferred for
terminating the attack immediately. Initially, when the patient is first seen, 10 mg diazepam (0.30.5 mg/kg bw) should be given slowly intravenously over a period of 2-5 minutes. Its action lasts
for 20-30 minutes. Lorazepam in doses of 0.1 mg/kg at 2 mg/minute is preferable to IV
Diazepam as it has longer duration of action (> 4 hrs) and lesser respiratory depression

NURSING MANAGEMENT
Assessment
Important health information
Past medical /surgical history
Birth defect or injuries
Cns trauma,tumors,or infection
Alcoholism,stroke,metabolic disorders,drug abuse etc
Physical examination

Nursing diagnosis
1, Ineffective breathing pattern related to neuromuscular impairment secondary to prolonged
tonic phase of seizure or during post ictal period as evidenced by abnormal respiratory
rate,rhythm and depth
INTERVENTIONS
Monitor respiratory and oxygenation status to determine presence and extent of problem
and to initiate appropriate interventions.
Postion the patient (side lying)to maximize ventilation potential.
Identify patient requiring actual/potential airway insertion to facilitate intubation as
necessary
Loosen clothing to prevent restricted breathing
Apply oxygen as appropriate to maintain oxygenation and prevent hypoxia.

2. Risk for injury related to seizure activity and subsequent impaired physical mobility secondary
to postictal weakness
INTERVENTIONS
Remove potential harmful objects from the environment.
Keep,suction,ambu bag,oral or nasopharyngeal airway at bedside to maintain airway
oxygenation if needed.
Use padded side rails to prevent injury during a seizure.
Record seizure characteristics ,body parts involved ,motor activity and seizure
progression.
Monitor post ictal period duration and characteristics to plan appropriate intervention as
needed.
3.Ineffective coping related to perceived loss of control and denial of diagnosis as evidenced
by verbalization bout not having epilepsy ,lack of truth telling regarding seizure frequency
,non compliant behavior.
INTERVENTIONS
Appraise the impact of patients life situation on roles and relationships to determine
extent of problem and to plan appropriate interventions.
Appraise and discuss alternative response to situation.
Provide factual information concerning diagnosis,treatment,and prognosis.
Arrange situations that encourage patients autonomy to promote effective coping by
providing correct information.
Describe rationale behind management /treatment recommendations.
4. Ineffective therapeutic regimen management related to lack of knowledge about
management of seizure disorder as evidenced by verbalization of lack of knowledge
,inaccurate perception of health status.

INTERVENTION
Discuss lifestyle changes (eg.avoidance of precipitating factors ,driving restriction
,wearing medical id tags,exposure to stress) that may be required to prevent future
complications and control of disease process .
Discuss therapy treatment options and describe rationale behind management
/treatement options so patient and family can make lifestyle modifications to manage
a chronic disease.
RECENT STUDIES RELATED TO EPILEPSY

FDA approves medical device to treat epilepsy (nov 2013)

The U.S. Food and Drug Administration approved a device to help reduce the frequency of
seizures in epilepsy patients who have not responded well to medications.

The RNS Stimulator consists of a small neurostimulator implanted within the skull under the
scalp. The neurostimulator is connected to one or two wires (called electrodes) that are placed
where the seizures are suspected to originate within the brain or on the surface of the brain.
The neurostimulator detects abnormal electrical activity in the brain and responds by delivering
electrical stimulation intended to normalize brain activity before the patient experiences seizure
symptoms, said Christy Foreman, director of the Office of Device Evaluation in the FDAs
Center for Devices and Radiological Health.
Epilepsy produces seizures affecting varied mental and physical functions. Seizures happen
when clusters of nerve cells in the brain signal abnormally, which may briefly alter a person's
consciousness, movements or actions. According to the Epilepsy Foundation, epilepsy affects
nearly 3 million people in the United States and is the third most common neurological disorder,
after Alzheimers disease and stroke. Approximately 40 percent of people with epilepsy are
severely affected and continue to have seizures despite treatment.
The FDAs approval is supported by a three-month randomized control trial of 191 patients with
drug-resistant epilepsy.
The study showed that by three months after the implanted device was turned on (active use)
patients experienced a nearly 38 percent reduction in the average number of seizures per month,
compared to an approximately 17 percent reduction in the average number of seizures per month
in patients who had the implanted device turned off. At the end of three months, the median
reduction in seizures, which reflects a more typical patient experience, was 34 percent with
active use and about 19 percent with the device turned off. During the trial, 29 percent of patients
with an active device experienced at least a 50 percent reduction in the overall number of
seizures, compared to 27 percent for those with the implanted device turned off.
During a two-year follow-up phase (unblinded), data demonstrated a persistent reduction in
seizure frequency.
Patients with RNS Stimulators cannot undergo magnetic resonance imaging (MRI) procedures,
nor can they undergo diathermy procedures, electroconvulsive therapy (ECT) or transcranial
magnetic stimulation (TMS). The energy created from these procedures can be sent through the
neurostimulator and cause permanent brain damage, even if the device is turned off.
The most frequent adverse events reported were implant site infection and premature battery
depletion.
The RNS Stimulator is manufactured by Neuropace, Inc. of Mountain View, Calif

A new treatment for drug-resistant epilepsy with the potential to suppress seizures on
demand with a pill, similar to how you might take painkillers when you feel a headache
coming on, has been developed by UCL researchers funded by the Wellcome Trust.
The treatment, described in Nature Communications, combines genetic and chemical approaches
to suppress seizures without disrupting normal brain function. The technique was demonstrated
in rodents but in future we could see people controlling seizures on-demand with a simple pill.
Epilepsy affects around 50 million people worldwide including 600,000 in the UK and around a
quarter of cases are resistant to conventional treatments. Many of these cases could be addressed
by the new treatment method, which relies on genetic modification of brain cells to make them
sensitive to a normally inactive compound.
First, we inject a modified virus into the area of the brain where seizures arise, explains
Professor Dimitri Kullmann of the UCL Institute of Neurology, senior author of the research.
This virus instructs the brain cells to make a protein that is activated by CNO (clozapine-Noxide), a compound that can be taken as a pill. The activated protein then suppresses the overexcitable brain cells that trigger seizures, but only in the presence of CNO.
At the moment, severe seizures are treated with drugs that suppress the excitability of all brain
cells, and patients therefore experience side effects. Sometimes the dose required to stop seizures
is so high that patients need to be sedated and taken to intensive care. If we can take our new
method into the clinic, which we hope to do within the next decade, we could treat patients who
are susceptible to severe seizures with a one-off injection of the modified virus, and then use
CNO only when needed.
If we can take our new method into the clinic, which we hope to do within the next decade, we
could treat patients who are susceptible to severe seizures with a one-off injection of the
modified virus, and then use CNO only when needed.
Professor Dimitri Kullmann (UCL Institute of Neurology)-